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The metallic nickel nanoparticle is a product with many new characteristics, which include a high level of surface energy, high magnetism, low melting point, high surface area, and low burning point. Therefore, it can be widely used in modern industries. However, metallic nickel nanoparticles may also initiate adverse health effects. Numerous studies have described the pathogenic and carcinogenic effects of nickel compounds, but little has been documented on the biological effects of metallic nickel nanoparticles. Activator protein-1 (AP-1) and nuclear factor-kB (NF-kB) have been shown to play pivotal roles in tumor initiation, promotion, and progression. The present study examines effects of metallic nickel particles on tumor promoter or suppressor genes and its signal transduction pathways in JB6 cells. Our results demonstrated that metallic nickel nanoparticles activated AP-1 and NF-kB more efficiently than nickel fine particles as investigated using luciferase assay, western blot, as well as immunocytochemistry staining. Further studies indicated that, compared to fine particles, nickel nanoparticles induced a higher level protein expression of c-myc and R-Ras in a time-dependent manner. Furthermore, nickel nanoparticles caused a greater decrease of p53 transcription activity than fine particles as demonstrated by luciferase assay. These findings suggest that nickel nanoparticles may exhibit higher carcinogenic potential than nickel fine particles. The results obtained from this study will be of benefit for elucidating the pathogenic and carcinogenic potential of metallic nickel nano- and fine particles. In addition, the results may be useful as a reference when comparing the carcinogenesis of different nickel compounds.